Insulin resistance is an intrinsic defect independent of fat mass in women with Turner's syndrome

Burak Salgin, Rakesh Amin, Kevin Yuen, Rachel M. Williams, Peter Murgatroyd, David B. Dunger

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

Background/Aims: Turner's syndrome (TS) is associated with increased insulin resistance and adiposity, which might be associated with type 2 diabetes in later life. We aimed to determine whether the defect in insulin sensitivity is a primary intrinsic defect in TS or dependent on variation in body composition. Methods: Sixteen women with TS not on growth hormone replacement but receiving oestrogen replacement therapy [age (mean ± SD): 30.2 ± 8.5 years; height-corrected fat-free mass: 26.1 ± 3.1 kg/height] and a control group of 16 normal healthy women (age: 30.1 ± 8.2 years; height-corrected fat-free mass: 25.9 ± 2.4 kg/height) were studied. Fasting blood samples were obtained for measurement of glucose, insulin, IGF-I, IGFBP-1, IGFBP-3 and lipid levels. The hyperinsulinaemic euglycaemic clamp was performed to assess peripheral insulin sensitivity (M value), and the Homeostasis Model Assessment (HOMA-S) was used to estimate fasting insulin sensitivity. Body composition was assessed using a dual-energy X-ray absorptiometry scan. Results: Fasting insulin sensitivity (HOMA-S 103.2 ± 78.6 vs. 193.9 ± 93.5, p = 0.006) was lower in TS subjects compared to controls as was whole-body insulin sensitivity (M value 2.9 ± 1.9 vs. 5.5 ± 2.6 mg/kg/min, p = 0.003). In a multiple regression analysis the Turner karyotype was significantly related to insulin sensitivity (p = 0.008) independent of any differences in fat-free mass and percent whole-body fat mass. Conclusion: The increased insulin resistance in women with TS is independent of measures of body composition and may represent an intrinsic defect related to their chromosomal abnormality.

Original languageEnglish (US)
Pages (from-to)69-75
Number of pages7
JournalHormone Research
Volume65
Issue number2
DOIs
StatePublished - Feb 2006
Externally publishedYes

Fingerprint

Turner Syndrome
Insulin Resistance
Fats
Body Composition
Fasting
Homeostasis
Insulin-Like Growth Factor Binding Protein 1
Insulin-Like Growth Factor Binding Protein 3
Estrogen Replacement Therapy
Glucose Clamp Technique
Photon Absorptiometry
Adiposity
Insulin-Like Growth Factor I
Karyotype
Chromosome Aberrations
Type 2 Diabetes Mellitus
Growth Hormone
Adipose Tissue
Regression Analysis
Insulin

Keywords

  • Body composition
  • Insulin resistance
  • Turner's syndrome

ASJC Scopus subject areas

  • Endocrinology

Cite this

Salgin, B., Amin, R., Yuen, K., Williams, R. M., Murgatroyd, P., & Dunger, D. B. (2006). Insulin resistance is an intrinsic defect independent of fat mass in women with Turner's syndrome. Hormone Research, 65(2), 69-75. https://doi.org/10.1159/000090907

Insulin resistance is an intrinsic defect independent of fat mass in women with Turner's syndrome. / Salgin, Burak; Amin, Rakesh; Yuen, Kevin; Williams, Rachel M.; Murgatroyd, Peter; Dunger, David B.

In: Hormone Research, Vol. 65, No. 2, 02.2006, p. 69-75.

Research output: Contribution to journalArticle

Salgin, B, Amin, R, Yuen, K, Williams, RM, Murgatroyd, P & Dunger, DB 2006, 'Insulin resistance is an intrinsic defect independent of fat mass in women with Turner's syndrome', Hormone Research, vol. 65, no. 2, pp. 69-75. https://doi.org/10.1159/000090907
Salgin, Burak ; Amin, Rakesh ; Yuen, Kevin ; Williams, Rachel M. ; Murgatroyd, Peter ; Dunger, David B. / Insulin resistance is an intrinsic defect independent of fat mass in women with Turner's syndrome. In: Hormone Research. 2006 ; Vol. 65, No. 2. pp. 69-75.
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